ABRUPTIO PLACENTA

BY
Dr. C.E. Enyindah
Dept of Obstetrics & Gynaecology
University of Port Harcourt
 DEFINITION

Bleeding following premature

separation of a
normally situated placenta
 AETIOLOGY
• This is not known, but there are some
associated factors which include:-
– Hypertension and severe pre-eclampsia
– Direct trauma
– High Parity
– Low socio-economic status
– Folic acid deficiency?
– Polyhydramnios
– Short umbilical cord
CLASSIFICATION
This is classified into three categories –
• Revealed type – the bleeding is
revealed.
• Concealed type – there is no obvious
bleeding
• Mixed type – a combination of
revealed and mixed.
CLINICAL PRESENTATION
Vaginal bleeding –
• This is either revealed or concealed. The
concealed form is more dangerous and is
associated with increasing pallor, shock,
abdominal pain, abdominal girth and
fundal height.
• Seepage of blood into the myometrium
and then to the peritoneal cavity results in
couvelaire uterus and haemoperitoneum
respectively.
• Serous fluid from the retro placental clot
may be confused with amniotic fluid.
• Ruptured membranes may reveal
bloodstained amniotic fluid.
Abdominal pain
Uterine tenderness.
Uterus may be woody hard and tender
rendering fetal parts difficult to palpate or
impalpable.
Fetal distress
Fetal death
Maternal shock/Death
 CLINICAL GRADING OF ABRUPTIO
PLACENTA
• The grading of Abruptio placenta according to
SHER and STUTLAND (1985) is as below
Grade Clinical features
I Not recognized clinically before delivery.
II Intermediate. The classical signs of abruption
are present but the fetus is still alive.
III Severe. The fetus is dead
a. Without Coagulopathy
b. With Coagulopathy
 DIAGNOSIS
This is made on clinical grounds but
ultrasonography may be helpful in a few
doubtful (mild) cases. Symptoms and
signs may be diagnostic for moderate to
severe cases but mild cases may pose
diagnostic difficulty until a retroplacental
clot is identified after delivery.
• The other ancillary investigations include –
– Full blood count
– Coagulation profile -
 • Clotting time, platelet count,
fibrinolysin test, fibrinogen estimation,
and FDP (Fibrinogen degradation
products)
• Acid base status (PH, blood gas analysis)
• Blood urea and electrolytes
• Urine microscopy, culture and sensitivity
 DIFFERENTIAL DIAGNOSIS
This must be considered in terms of causes of vaginal
bleeding and causes of abdominal pain e.g.
• Abdominal pains
– Acute appendicitis
– Pyelonephritis
– Twisted ovarian cyst
– Red-degenerating uterine fibroid
– Retroperitoneal haemorrhage
– Rectus sheath haematoma
– Chorioamnionitis
– Lumbar or sacral strain
– Ruptured uterus
• Vaginal bleeding
– Placenta praevia
– Vasa praevia
 COMPLICATIONS
• Maternal
– Hypovolaemic shock
– Acute renal failure – result of haemorrhagic shock,
acute renal tubular and cortical necrosis and DIC
– DIC – from thromboplastin release or excessive blood
loss.
– PPH – from DIC or from couvelaire uterus.
– Fetomaternal haemorrhage. May result in rhesus
sensitization in Rh (D) negative women.
– Maternal mortality
 FETAL
• IUGR
• Congenital malformations
• Abnormal neonatal haematology –
anaemia and transient coagulopathies.
• Perinatal mortality (FSB and ENND)
 MANAGEMENT
• This depends on severity, associated
complications, state of the patient, state of
the fetus and the gestational age.
• General management – resuscitation.
• Specific measures –
– Immediate delivery
– Expectant management
– Management of complications.
 A IMMEDIATE DELIVERY
Depends on the severity of the abruption,
and the state of the fetus (dead or alive)
 i) DEAD FETUS
• Aim at vaginal delivery
• Needs adequate resuscitation with IV fluids,
blood and plasma.
• ARM plus or minus oxytocin (with oxytocin, close
monitoring to avoid over stimulation and uterine
rupture). Where there is the least doubt about
the diagnosis, perform ARM in theatre in case
there is a concomitant placenta praevia.
• Delivery should be effected within 6 hrs. If
bleeding continues and progress of labour is
slow, deliver by C/S. Note that C/S is risky in
the presence of DIC. If there is not much blood
available to resuscitate the patient adequately,
then early recourse to C/S may be justifiable.
 ii) LIVE FETUS
• CS or vaginal delivery. CS offers better
chances of survival for the baby. If vaginal
delivery is aimed at, then there is the need
for continuous fetal electronic monitoring
and this may be considered if labour is
well advanced. This is not possible in our
environment.
• Fetal distress – immediate CS
B EXPECTANT MANAGEMENT
This may be done for very mild cases in
which the fetus is immature. Such cases
may develop mild localized tenderness
over the uterus. The ultrasound scan
identifies a small retroplacental clot.
• Admit patient
• Pain relief
• Continuous electronic fetal heart rate
monitoring (if available)
• Repeated USS for first few hours to monitor rate
of progression of retroplacental clot.
• Monitor fetus subsequently by –
– Daily fetal kick counts
– Twice weekly CTG
– Twice weekly ultrasound scan.
• If abruption progresses, deliver as soon as
possible.
• If abruption does not progress, continue
expectant management till 37 wks and deliver.
C MANAGEMENT OF COMPLICATIONS
Haemorrhagic Shock
• The tendency is to underestimate blood loss due
to concealed Abruptio placenta.
• The aim of treatment is to restore effective blood
volume and hence tissue perfusion.
This involves the following –
– Setting up IV line /collecting blood for investigations.
– IV fluids – colloids/crystalloids.
– Oxygen by face-mask.
– Monitor of fluid replacement to avoid overload.
– Watch out for problems of massive transfusion.
 2 DISSEMINATED INTRAVASCULAR
COAGULATION (DIC)
More common in severe abruption or
massive haemorrhage. There are three
stages based on laboratory
measurements and clinical features –
– Low grade and compensated.
– Uncomplicated, no haemostatic failure
– Rampant with haemostatic failure
Treatment Involves
• Delivery of the fetus / placenta
• Replacement of lost blood and consumed factors;
via fresh whole blood / FFP / Packed cells.
 3. RENAL FAILURE
Caused by hypovolaemic shock and intravascular
clotting in the kidneys from DIC. Types of renal
damage are acute tubular necrosis and acute
cortical necrosis.
Treatment entails –
– Consult to renal physician.
– Fluid replacement / renal function monitoring.
– Diuretics (manitol 20% and IV frusemide)-Use with
caution..
 4. PPH
• Treatment involves
– Adequate blood transfusion
– Use of oxytocics – ergometrine, oxytocin,
syntometrine and PGF2a
– Internal iliac artary ligation or hysterectomy
– Rh-sensitisation
THANK YOU